This invention relates generally to programmable cardiac stimulating devices. More specifically, the present invention is directed to an implantable stimulation device and associated method that allow for the selection of an inter-atrial or inter-ventricular stimulation delay which results in optimal hemodynamic benefit for the patient.
In the normal human heart, the sinus node, generally located near the junction of the superior vena cava and the right atrium, constitutes the primary natural pacemaker initiating rhythmic electrical excitation of the heart chambers. The cardiac impulse arising from the sinus node is transmitted to the two atrial chambers, causing a depolarization known as a P-wave and the resulting atrial chamber contractions. The excitation pulse is further transmitted to and through the ventricles via the atrioventricular (A-V) node and a ventricular conduction system causing a depolarization known as an R-wave, also referred to as the QRS complex, and the resulting ventricular chamber contractions. Disruption of this natural pacemaking and conduction system as a result of aging or disease can be successfully treated by artificial cardiac pacing using implantable cardiac stimulation devices, including pacemakers and implantable defibrillators, which deliver rhythmic electrical pulses or other anti-arrhythmia therapies to the heart at a desired energy and rate. One or more heart chambers may be electrically stimulated depending on the location and severity of the conduction disorder.
Cardiac pacemakers conventionally stimulate a heart chamber by applying current pulses to cardiac tissues via two electrodes, a cathode and an anode. Standard pacing leads are available in either of two configurations, unipolar leads or bipolar leads. A unipolar lead has a single cathodic electrode with the anode being the pacemaker housing. A bipolar lead possesses two electrodes located 1 to 2 cm apart.
A single-chamber pacemaker delivers pacing pulses to one chamber of the heart, either one atrium or one ventricle, via either a unipolar or bipolar lead. Single-chamber pacemakers can operate in either a triggered mode or a demand mode. In a triggered mode, a stimulation pulse is delivered to the desired heart chamber at the end of a defined time-out interval to cause depolarization of the heart tissue (myocardium) and its contraction. The stimulating pulse must be of sufficient energy to cause depolarization of the heart chamber, a condition known as xe2x80x9ccapture.xe2x80x9d The lowest pulse energy required to achieve capture is termed xe2x80x9cthreshold.xe2x80x9d The pacemaker also delivers a stimulation pulse in response to a sensed event arising from that chamber when operating in a triggered mode.
When operating in a demand mode, sensing and detection circuitry allow for the pacemaker to detect if an intrinsic cardiac depolarization, either an R-wave or a P-wave, has occurred within the defined time-out interval. If an intrinsic depolarization is not detected, a pacing pulse is delivered at the end of the time-out interval. However, if an intrinsic depolarization is detected, the pacing pulse output is inhibited to allow the natural heart rhythm to preside. The difference between a triggered and demand mode of operation is the response of the pacemaker to a detected native event.
Dual chamber pacemakers are now commonly available and can provide either trigger or demand type pacing in both an atrial chamber and a ventricular chamber, typically the right atrium and the right ventricle. Both unipolar or bipolar dual chamber pacemakers exist in which a unipolar or bipolar lead extends from an atrial channel of the dual chamber device to the desired atrium (e.g. the right atrium), and a separate unipolar or bipolar lead extends from a ventricular channel to the corresponding ventricle (e.g. the right ventricle). In dual chamber, demand-type pacemakers, commonly referred to as DDD pacemakers, each atrial and ventricular channel includes a sense amplifier to detect cardiac activity in the respective chamber and an output circuit for delivering stimulation pulses to the respective chamber. If an intrinsic atrial depolarization signal (a P-wave) is not detected by the atrial channel, a stimulating pulse will be delivered to depolarize the atrium and cause contraction. Following either a detected P-wave or an atrial pacing pulse, the ventricular channel attempts to detect a depolarization signal in the ventricle. If no R-wave is detected within a defined atrial-ventricular interval (AV interval or AV delay), a stimulation pulse is delivered to the ventricle to cause ventricular contraction. In this way, rhythmic dual chamber pacing is achieved by coordinating the delivery of ventricular output in response to a sensed or paced atrial event.
Over the years, dual-chamber stimulation has been found to provide clinical benefit to patients suffering from congestive heart failure and other cardiac abnormalities. It has also been found that the optimization of timing intervals during stimulation may be critical in providing hemodynamic benefit. Numerous schemes for optimizing the AV delay in order to improve cardiac function have been proposed. Reference is made, for example, to U.S. Pat. No. 5,540,727 to Tockman et al; U.S. Pat. No. 5,584,868 to Salo et al.; and U.S. Pat. No. 6,044,298 to Salo et al. Such schemes often incorporate sensors designed to assess cardiac function by monitoring blood pressure, pulse pressure, cardiac impedance, cardiac wall motion, heart sounds and other similar parameters.
In patients suffering from congestive heart failure, dilation of the heart can alter normal conduction pathways. Conduction through the heart chambers can become slower or inter-atrial or inter-ventricular conduction delays can develop. Thus, synchronizing the right and left heart chambers during bi-ventricular, bi-atrial, or multi-chamber stimulation may be vital to improving cardiac output. Mounting clinical evidence supports the evolution of more complex cardiac stimulating devices capable of stimulating three or even all four heart chambers to stabilize arrhythmias or to re-synchronize heart chamber contractions (see Cazeau S. et al., xe2x80x9cFour chamber pacing in dilated cardiomyopathy,xe2x80x9d Pacing Clin. Electrophsyiol 1994 17(11 Pt 2):1974-9).
One limitation of some multi-chamber stimulation systems is that stimulation of left and right heart chambers is simultaneous. Simultaneous contraction of both left and right chambers is not physiological and is not always necessary or desirable in a given patient. Proposed systems provide a delay between the stimulation of opposing heart chambers. Reference is made to U.S. Pat. No. 5,720,768 to Verboven-Nelissen; U.S. Pat. No. 5,902,324 to Thompson et al.; and U.S. Pat. No. 6,122,545 to Struble et al. While programmable inter-ventricular or inter-atrial delay intervals have been proposed, the selection of such intervals may be arbitrary.
Ideally, a direct measure of cardiac hemodynamics would be the best way to monitor the benefit of stimulation and provide feedback for making adjustments to stimulation timing intervals. However, direct measures such as left ventricular ejection fraction are impossible to perform chronically at the present time. Methods proposed previously for optimizing AV delay during dual chamber stimulation directed at maximizing hemodynamic performance are limited by the need for additional sensors and more complex software algorithms and may not apply to the optimization of inter-atrial timing or inter-ventricular timing.
Therefore, there remains an unmet need for a multi-chamber cardiac stimulation device that allows for the selection of an inter-atrial or inter-ventricular delay that results in optimal hemodynamic benefit for the patient. It would thus be desirable to provide automatic optimization of the delay between left and right heart chamber stimulation that could be adaptive over time, thereby adjusting the stimulation delay as needed with changes in disease state. It would also be desirable to provide such automatic, adaptive adjustment of this stimulation delay without requiring additional sensors or complex hardware.
The present invention addresses these needs by providing a method for optimizing the ventricular (or atrial) interpulse delay, that is the time between left and right ventricular (or atrial) chamber pulse delivery, during biventricular (or biatrial) stimulation. The present invention advantageously measures the width of the QRS complex. Since a narrow QRS complex, that is a relatively short ventricular depolarization signal, generally implies a more uniform contraction of the right and left ventricles, a more uniform contraction is associated with a more effective hemodynamic performance of the cardiac stimulation device.
Conduction abnormalities that cause inter- or intra-ventricular conduction delays produce less synchronized contractions of the right and left ventricles that can be recognized by a widened QRS complex. Thus, by monitoring the QRS width in response to different interpulse delays during biventricular stimulation, the optimal interpulse delay setting that results in the minimum QRS width and presumably the most optimal hemodynamic benefit can be determined.
Thus, one feature of the present invention is a method for sensing and measuring the QRS width. Sensing the QRS complex may be done using the same electrodes used for stimulating the ventricles (near-field sensing), but preferably is done using electrodes that are not in direct contact with the ventricles (far-field sensing) in order to make a global measurement of the ventricular depolarization.
Another feature of the present invention is an algorithm that allows comparisons of the QRS width measured during biventricular stimulation at different interpulse delays. Preferably a convergent, iterative algorithm is used to identify the interpulse delay producing the minimum QRS width.
Yet another feature of the present invention is the adaptive adjustment of the interpulse interval over time. Since changes in disease state, medical therapy, physical activity or other factors may cause changes in the electromechanical response of the heart, the optimal interpulse interval may change over time. Therefore, the present invention includes periodic, automatic execution of the interpulse delay optimization algorithm so that the interpulse delay is automatically adjusted over time, as needed.
In still another embodiment of the invention, the width of P waves are measured during biatrial pulsing. An optimal interpulse delay is selected by determining the P wave having the minimum width, and selecting the associated interpulse delay that caused such P wave.